Stroke, Vol 18, 1141-1147, Copyright © 1987 by American Heart Association
RK Simpson Jr and DS Baskin
Corticomotor evoked potentials have recently been used in experimental
animals and patients as a measure of neurologic function after stroke.
However, little is known about the fundamental electrophysiologic
properties contributing to the formation of these potentials. To define
some of these properties, corticomotor evoked potentials were recorded from
the contralateral hindlimb in response to transcortical stimulation in cats
anesthetized with halothane. These potentials were obtained hourly for 6
hours after middle cerebral artery occlusion. Four major identifiable
components were recorded in control responses. Immediately after
infarction, all component amplitudes were significantly attenuated.
However, after approximately 5 hours, the early latency components exceeded
control values; late latency components were also increased. Corresponding
somatosensory evoked potentials were abolished and did not return
throughout the recording session. Based on classic neurophysiologic
studies, the amplitude increment can be explained as combined activation of
low-threshold brainstem facilitatory centers and/or direct activation of
subcortical axonal pathways. With further study, corticomotor evoked
potentials may be a valuable adjunct to current electrophysiologic
monitoring techniques, particularly with regard to defining the extent and
location of an infarct, as well as to assessing functional recovery.
ARTICLES
Early component changes in corticomotor evoked potentials following experimental stroke
Section of Neurosurgery, Veterans Administration Hospital, Houston, Tex.
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